Tissue-Specific Stem Cells

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Human Gingiva-Derived Mesenchymal Stem Cells Elicit Polarization of M2 Macrophages and Enhance Cutaneous Wound Healing†‡§

  1. Qun-Zhou Zhang1,
  2. Wen-Ru Su1,
  3. Shi-Hong Shi1,
  4. Petra Wilder-Smith2,
  5. Andy Peng Xiang3,
  6. Alex Wong4,
  7. Andrew L. Nguyen1,
  8. Chan Wook Kwon1,
  9. Anh D. Le1,¶,*

Article first published online: 26 OCT 2010

DOI: 10.1002/stem.503

Issue

STEM CELLS

STEM CELLS

Volume 28, Issue 10, pages 1856–1868, October 2010

Additional Information

How to Cite

Zhang, Q.-Z., Su, W.-R., Shi, S.-H., Wilder-Smith, P., Xiang, A. P., Wong, A., Nguyen, A. L., Kwon, C. W. and Le, A. D. (2010), Human Gingiva-Derived Mesenchymal Stem Cells Elicit Polarization of M2 Macrophages and Enhance Cutaneous Wound Healing. STEM CELLS, 28: 1856–1868. doi: 10.1002/stem.503

Author Information

  1. 1

    Center for Craniofacial Molecular Biology, The Herman Ostrow School of Dentistry of University of Southern California, Los Angeles, California, USA

  2. 2

    Beckman Laser Institute, University of California, Irvine, California, USA

  3. 3

    Center for Stem Cell Biology and Tissue Engineering, Sun Yat-Sen University, Guangzhou, People's Republic of China

  4. 4

    Division of Plastic and Reconstructive Surgery, University of Southern California Keck School of Medicine, Los Angeles, California, USA

  1. Telephone: 323-442-2556; Fax: 323-442-2981

*Division of Endodontics, Oral & Maxillofacial Surgery & Orthodontics, Center for Craniofacial Molecular Biology, The Herman Ostrow School of Dentistry of University of Southern California, Health Sciences Campus, 2,250 Alcazar Street, CSA107, Los Angeles, California 90,033, USA

  1. †

    Author contributions: Q.-Z.Z.: conception and design, collection and assembly of data, manuscript writing, final approval of the manuscript; W.-R.S.: collection and assembly of data, final approval of the manuscript; S.-H.S.: collection and assembly of data; P.W.S.: manuscript writing, final approval of the manuscript; A.P.X.: manuscript writing, final approval of the manuscript; A.W.: manuscript writing, final approval of the manuscript; A.L.N: collection and assembly of data; B.K.: collection and assembly of data; A.D.L.: conception and design, manuscript writing, final approval of the manuscript, financial support.

  2. ‡

    Disclosure of potential conflicts of interest is found at the end of this article.

  3. §

    First published online in STEM CELLS EXPRESS August 23, 2010.

  4. Telephone: 323-442-2556; Fax: 323-442-2981

Publication History

  1. Issue published online: 26 OCT 2010
  2. Article first published online: 26 OCT 2010
  3. Accepted manuscript online: 23 AUG 2010 12:00AM EST
  4. Manuscript Accepted: 11 AUG 2010
  5. Manuscript Received: 2 JUN 2010

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Keywords:

  • Human gingival;
  • Mesenchymal stem cells;
  • M2 macrophages;
  • Wound healing

Abstract

Increasing evidence has supported the important role of mesenchymal stem cells (MSCs) in wound healing, however, the underlying mechanism remains unclear. Recently, we have isolated a unique population of MSCs from human gingiva (GMSCs) with similar stem cell-like properties, immunosuppressive, and anti-inflammatory functions as human bone marrow-derived MSCs (BMSCs). We describe here the interplay between GMSCs and macrophages and the potential relevance in skin wound healing. When cocultured with GMSCs, macrophages acquired an anti-inflammatory M2 phenotype characterized by an increased expression of mannose receptor (MR; CD206) and secretory cytokines interleukin (IL)-10 and IL-6, a suppressed production of tumor necrosis factor (TNF)-α, and decreased ability to induce Th-17 cell expansion. In vivo, we demonstrated that systemically infused GMSCs could home to the wound site in a tight spatial interaction with host macrophages, promoted them toward M2 polarization, and significantly enhanced wound repair. Mechanistically, GMSC treatment mitigated local inflammation mediated by a suppressed infiltration of inflammatory cells and production of IL-6 and TNF-α, and an increased expression of IL-10. The GMSC-induced suppression of TNF-α secretion by macrophages appears to correlate with impaired activation of NFκB p50. These findings provide first evidence that GMSCs are capable to elicit M2 polarization of macrophages, which might contribute to a marked acceleration of wound healing. STEM CELLS 2010;28:1856–1868

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